Ask about this productRelated genes to: AKT1 Blocking Peptide
- Gene:
- AKT1 NIH gene
- Name:
- AKT serine/threonine kinase 1
- Previous symbol:
- -
- Synonyms:
- RAC, PKB, PRKBA, AKT
- Chromosome:
- 14q32.33
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: AKT1 Blocking Peptide
Related articles to: AKT1 Blocking Peptide
- Spinal Cord Injury (SCI) is a highly disabling disease owing to unexpected mechanical damage, which may trigger serious complications. Tauroursodeoxycholic Acid (TUDCA) serves as a neuroprotective agent for SCI. Therefore, this study assessed the effect of TUDCA for intervening in SCI in existing preclinical tests, with a summary of its mechanism simultaneously. - Source: PubMed
Publication date: 2026/08/24
Wang Yi-XuanZhang Jia-XuanZhang Meng-JieXiao YuLi Zhuo-YaoZhang Bi-MengWang Yong-JunCui Xue-JunZhou Ai-FangYao Min - Shao Kuiling Decoction (SKD) is used in the long-term management of Ulcerative Colitis (UC), but its molecular basis remains unclear. Because SKD is a multicomponent formula, a computational approach is useful for identifying candidate compounds, targets, and pathways for further validation. - Source: PubMed
Publication date: 2026/08/21
Wu XiaoyunHe ZhiguangRen WeitaoZhao BinTseng Yuheng - Huangqin Qingre Chubi Capsules(HQC) are commonly used in clinical practice to treat rheumatoid arthritis(RA). It is composed of Scutellariae Radix, Gardeniae Fructus, Coicis Semen, Clematidis Radix et Rhizoma, and the stir-fried Persicae Semen. However, the pharmacological substance basis and mechanism are not yet clear. This study systematically elucidated the pharmacological substance basis and mechanism of HQC by the research strategy of "identification of target tissue migration components-network mechanism prediction-multidimensional experimental verification". An adjuvant-induced arthritis(AA) rat model was established, and the serum and synovium migration components of HQC in normal and AA model rats were analyzed using ultra-high performance liquid chromatography-quadrupole time-of-flight mass spectrometry(UPLC-Q-TOF-MS/MS). These serum and synovium migration components were integrated for network pharmacology prediction, which was followed by multi-dimensional validation using molecular docking, RT-qPCR, and pharmacodynamic evaluation. The results showed that 46 serum and 13 synovium migration components were identified in normal rats, and 59 serum and 15 synovium migration components were identified in AA rats, indicating that the RA disease environment affects the entry of HQC into the bloodstream and migration to the synovium. Comparative analysis of components common and unique to normal and model groups identified geniposide, baicalin, daucosterol, coptisine, acteoside, luteolin, and crocin as migration components reaching the target site, reflecting the target tissue enrichment characteristics of HQC. Network pharmacology of the migration components screened 7 core targets: GAPDH, TNF-α, AKT1, PTGS2, NF-κB1, MAPK1, and SphK1, which were enriched in key RA signaling pathways including PI3K-AKT, HIF-1, VEGF, and TNF. Molecular docking and RT-qPCR confirmed good binding activity and regulatory capacity between key components and core targets. In vivo validation further demonstrated that HQC significantly improved joint inflammation and synovial hyperplasia in AA rats. This study confirmed that HQC exerted an anti-RA effect by targeting chronic inflammation and metabolic disorders through multi-target regulation of PI3K-Akt and other signaling pathways via serum and synovium migration components. The research provides a scientific basis for the clinical application of HQC and offers a new strategy for studying the mechanisms of TCM. - Source: PubMed
Pang JingGan Pei-RongZhu Yu-LongWang YingBu Yan-HongWu Hong - To identify clinically advantageous TCMs for anti-hepatic fibrosis and to elucidate the effects and molecular mechanisms of Salvia miltiorrhiza ethanol extract in the intervention of liver fibrosis, this study screened high-frequency anti-hepatic fibrosis TCMs through a review of clinical literature. The S. miltiorrhiza active components, potential targets, and liver fibrosis-related disease targets were obtained using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP), the GeneCards database, and other databases. Gene Ontology(GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses were performed on the shared targets between drugs and diseases. Molecular docking was conducted to evaluate the binding affinities between key components and core targets. In animal experiments, male Kunming mice were used to establish a liver fibrosis model induced by carbon tetrachloride(CCl_4). The mice were administered low, medium, and high doses of S. miltiorrhiza ethanol extract by gavage. The liver index, as well as serum aspartate aminotransferase(AST) and alanine aminotransferase(ALT) levels, were measured. Histopathological changes in liver tissue were observed using hematoxylin-eosin(HE) staining and Masson's trichrome staining. Western blot analysis was used to detect the protein expression levels of α-smooth muscle actin(α-SMA), Collagen Ⅰ, and heat shock protein 90 alpha family class A member 1(HSP90AA1) in liver tissue. The results showed that S. miltiorrhiza was the most frequently used TCM in clinical anti-hepatic fibrosis. A total of 65 active components and 135 potential targets were identified, and 109 common targets were obtained by intersecting these with liver fibrosis-related targets. The core targets included tumor protein p53(TP53), serine/threonine protein kinase AKT1(AKT1), Jun proto-oncogene(JUN), signal transducer and activator of transcription 3(STAT3), and HSP90AA1, which were mainly enriched in pathways related to cancer, hepatitis B, and the PI3K-AKT signaling pathway. Molecular docking indicated that the main active components of S. miltiorrhiza bound stably to the core targets, with the strongest binding affinity observed for HSP90AA1. Animal experiments demonstrated that the liver index, serum ALT and AST levels, and the expression of α-SMA, Collagen Ⅰ, and HSP90AA1 in liver tissue were significantly increased in the model group, accompanied by obvious pathological manifestations of fibrosis. Compared with the model group, different dose groups of S. miltiorrhiza ethanol extract reduced the liver index and serum ALT and AST levels to varying degrees, alleviated pathological damage and collagen deposition in liver tissue, and downregulated the protein expression of α-SMA, Collagen Ⅰ, and HSP90AA1. In conclusion, S. miltiorrhiza ethanol extract exerts a significant protective effect on CCl_4-induced liver fibrosis in mice, and its mechanisms may be related to the inhibition of HSP90AA1 expression and the regulation of liver fibrosis-related signaling pathways. - Source: PubMed
Li JieLi Xiao-PiaoMiao Ling-RuiZou YiWen Li-YanLiao Shang-GaoHe XunZhang Jin-Juan - Hepatic fibrosis (HF) is a crucial and reversible stage, yet there is a paucity of effective clinical antifibrotic drugs. Salvianic acid A (SAA) has shown antifibrotic potential in preliminary studies; however, its molecular mechanisms and potential targets remain incompletely understood. To evaluate the therapeutic efficacy and mechanisms of SAA in mitigating HF, we employed a carbon tetrachloride (CCl)-induced HF mouse model. In parallel, we used transforming growth factor beta 1 (TGF-β1)-stimulated LX-2 cells and primary mouse hepatic stellate cells (HSCs) for in vitro studies. In CCl-induced mice, SAA markedly improved liver function and suppressed HF, as evidenced by significant reduction in α-smooth muscle actin and collagen I expression and alleviation of inflammatory response. Similar antifibrotic and anti-inflammatory effects were observed in vitro. To investigate the targets and mechanism of SAA in HF, we employed network pharmacology, molecular docking, molecular dynamics simulations, and microscale thermophoresis. We found that SAA was predicted to interact with the allosteric pocket of RAC-alpha serine/threonine-protein kinase 1 (AKT1), accompanied by inhibition of AKT1 phosphorylation and the downstream nuclear factor-kappa B (NF-κB) signaling. To further explore the involvement of AKT1 in SAA's antifibrotic effects, we used the AKT activator SC79. In CCl-induced mice, SC79 partly reversed the antifibrotic effects of SAA. Consistently, we observed that SC79 partially restored the inflammatory and fibrotic markers in TGF-β1-simulated HSCs, counteracting the inhibitory efficacy of SAA. Our findings suggest that SAA exerts antifibrotic effects in part through suppression of the AKT1/NF-κB axis and may represent a promising therapeutic candidate for HF. - Source: PubMed
Publication date: 2026/09/03
Hu JinqiZhang JiexinGe XiaomeiLi SuyuLi XudongZhang TianruiLi XiangHe MengGao GuanbinSun Taolei